Just to add on to what Vascular stated. The protease in hibitors block the action of cellular and viral proteases that aid in asembly of the viroid. Non-nucleoside inhibtors, encompass a broad spectrum, but normally inhibit dimer formation of reverse transcriptase or thymidine kinase inhibition like ratonovir and acyclovir. Nucleoside inhibitors, aka chain terminators like AZT, stop DNA synthesis (and hence proviral integration into the genome).
The three are very effective when used together. However resistance, especially to the protease inhibitors, is being more of a problem.
Huge strides are being made in the non-nucleoside portion, but the others have kind of jit a dead end. The future of treatments will be with synthetic peptides and antibodies that interfere with the viral life cycle.